Question 11

College Answer

a)

Pulsus paradoxus is an exaggeration (> 12 mmHg or 10%) of the normal inspiratory decrease in systemic blood pressure.

Decreased intrathoracic pressure with inspiration results in increased venous return to right heart and bulge of IVS to left. Because the ventricle can normally also expand outward, this septal shift is usually small, and the difference in the blood pressure is therefore small between inspiration and expiration (<10 mmHg). With tamponade, the left ventricle cannot expand outward, so the septal shift is exaggerated and the difference in BP is larger. Also, the relatively higher negative pressure in the pulmonary circulation compared to the left atrium in patients with pericardial pathology pooling of blood in pulmonary veins during inspiration resulting in decreased LV stroke volume.

b)

Palpation of pulse- disappears in deep inspiration

Sphygmomanometer- Korotkoffs sounds first heard in expiration only and then in inspiration with progressive deflation

Pulse Oximeter-particularly useful in paediatrics

Arterial pressure trace- exaggerated fall of systolic pressure in inspiration

c)

Hypotension

Elevated JVP (neck vein distension with inspiration- Kussmaul’s sign) Muffled heart sounds

Tachypnoea

Exaggerated drop in diastolic CVP (Friedrich’s sign)

Absent y descent on CVP trace

Clinical signs of shock- decreased peripheral perfusion, slow capillary refill, oliguria, confusion.

d)

Tachycardia

Low QRS voltage trace Electrical alternans

Global concave ST elevation PR depression

e)

Visible pericardial effusion

Diastolic collapse of Right Atrium and Right Ventricle

Respiratory variation in left and right sided volumes. Atrial and ventricular septa move leftward during inspiration and rightward during expiration

Mitral and Tricuspid flow velocities are increased and out of phase. Mitral flow is increased on the first beat of inspiration and tricuspid flow is increased on expiration.

The IVC is distended and does not collapse on inspiration

Discussion

a) The definition of pulsus paradoxus used by the college is from Curtiss et al (1988) who demonstrated that 12 mmHg and 9% systolic variation (not 10%) are the 95% confidence limits for diagnosis of moderate or severe tamponade. Most textbooks instead use 10mmHg as a convenient round number, described by Swami and Spodick (2003) as "a quasi arbitrary but practical level".

b) there are in fact only four methods known:

• Invasive arterial pressure trace: that's the classical ICU technique of demonstrating pulsus paradoxus, and is colloquially described as a "swing" of the arterial line.
• Palpation of the radial pulse:  the disappearance of the radial pulse on inspiration was the original sign described by Kussmaul.
• Sphygmomanometry: with the blood pressure measurement cuff inflated to the level of the systolic blood pressure, one ought to hear Korotkoff sounds.  Because the systolic blood pressure falls during spontaneous inspiration, the Korotkoff sounds disappear during inspiration. 
• Pulse oximetry is "particularly useful in paediatrics" according to the college examiners; they probably said this on the basis of a study by Tamburro et al (2002). The pulse oximeter waveform does something similar to the waveform of an arterial line, i.e "a decrease in the highest value of the upper plethysmographic peak of the pulse-oximetry waveform was observed during inspiration in each patient". Tamburro et al  observed this phenomenon in eight children and adolescents, which might give rise to the impression that this technique is "particularly useful in paediatrics". This might be in reference to the practical difficulties of using invasive blood pressure monitoring in children; otherwise the technique is probably equally useful in adults. 

c) These are the clinical signs of cardiac tamponade (some available mainly via invasive monitoring waveforms)

• Nonspecific findings which include tachycardia and tachypnoea

• Beck's Triad: Muffled heart sounds, hypotension and raised CVP.
• Kussmaul's sign: the neck veins distend with inspiration, instead of collapsing (though not everybody agrees that this is seen in tamponade)
• Friedreich's sign: an exaggerated early drop in diastolic CVP.
• Pulsus paradoxus - an exaggeration of the normal inspiratory fall in blood pressure
• Pericardial rub  if the tamponade is associated with some sort of pericardial inflammation
• Pericardial "knock", first described by Maynard Smith  (consulting surgeon of the British Expeditionary Force, 1918)  as a sound which  "may be compared to that heard in the ear-piece of a telephone when the lever is moved up and down". 
• A third heart sound 
• Displaced apex beat 
• Characteristric CVP findings: classically, a sawtooth "M" or "W"  configuration of a raised CVP.
  
  In summary
  • The CVP is raised
  • All CVP waveform components are elevated
  • a and v waves are tall
  • x descent is steep
  • y descent is (usually) absent

d) Electrocardiograhic features of pericarditis with tamponade are:

• Tachycardia 
• Low QRS voltage trace - which develops as the result of a large volume of fluid in the way between the heart and the electodes, a fluid which has relatively poor conductivity. Not surprisingly, this feature is found more often in patients with large effusions. However,  truly humongous effusions can be present without any tamponade physiology. 
• Electrical alternans  is the presence of alternating high and low QRS complexes. LITFL has a nice example. 
• Global concave ST elevation results from the current of injury which develops from direct pressure on the myocardium. 
• PR depression - this is usually asociated with pericarditis, and because pericarditis is often associated with pericardial effusion the PR segments are often depressed in cardiac tamponade. Obviously, cardiac tamponade which is not due to pericarditis will probably have normal-looking PR segments. 
• T wave inversion may develop as a result of pericardial irritation, but is by no means unique to cardiac tamponade. 

e) Echocardiographic features listed here are from Pérez-Casares et al (2017) 

• A visible pericardial effusion is certainly a helpful finding but is by no means mandatory. Particular examples of tamponade without a significant effusion might include blood clot following cardiac surgery, where the clot does not present as a classical black echolucency you'd normally expect of a pericardial effusion.
• Diastolic collapse of right atrium and right ventricle: this happens when the intra-chamber pressures are at their lowest. In diastole, there will be a timer where the chamber pressures are actually lower than the pericardial fluid pressure. In this situation the chambers will collapse. Atrial collapse is usually seen before ventricular collapse
• Right atrial collapse in systole:  in early systole, atrial cavity pressure  is lower than the pericardial fluid pressure, and there is collapse of the thin free wall. Duration of this phenomenon is important: apparently, collapse for longer than one-third of the cardiac cycle is 100% specific for clinical cardiac tamponade
• Right ventricular collapse in diastole: during the early stages, this is only present in expiration when venous return is at its poorest. Again, the loger the duration of collapse, the more severe the tamponade.
• Diastolic ventricular size variability with respiratory cycle  is visually demonstrated using M-mode. Inspiration brings venous return to the RV and the RV dilates, pushing the septum into the LV. The opposite occurs in expiration. 
• Septal "bounce" is the colloquial-sounding name given to the inspiratory movement of the septum towards the LV. 
• IVC dilatation is seen because all the veins are dilated, and is essentially the echocardiographic equivalent of a raised JVP.
• Mitral flow is decreased on inspiration:  in cardiac tamponade the peak E-wave velocity is decreased by 25% on inspiration.
• Peak E-wave tricuspid valve physiological variation is larger than the mitral valve fluctuations -  in tamponade the peak E-wave velocity will drop by 40% in expiration compared to inspiration.
• RVOT/LVOT flow velocity fluctuation:  during normal respiration the physiologic variation of flow in these regions is less than 10%, but in tamponade the fluctuation is greater. During inspiration the aortic peak velocity will drop by 10%, and a rise of 10% will be seen in the pulmonary trunk.
• Hepatic vein flow reversal: in diastole, before atrial contraction the flow is either slowed or reversed. 
• Pulmonary vein flow reversal: again the flow is either slowed or reversed before the atria contract (usually there would be some flow reversal when the atria contract, which is perfectly normal physiological phenomenon)

Beck, Claude S. "Two cardiac compression triads." Journal of the American Medical Association 104.9 (1935): 714-716.

Spodick, David H. "Acute cardiac tamponade." New England Journal of Medicine 349.7 (2003): 684-690.

Ariyarajah, Vignendra, and David H. Spodick. "Cardiac tamponade revisited: a postmortem look at a cautionary case." Texas Heart Institute Journal 34.3 (2007): 347.

Bilchick, Kenneth C., and Robert A. Wise. "Paradoxical physical findings described by Kussmaul: pulsus paradoxus and Kussmaul's sign." The Lancet 359.9321 (2002): 1940-1942.

Lange, Ramon L., et al. "Diagnostic signs in compressive cardiac disorders: constrictive pericarditis, pericardial effusion, and tamponade." Circulation 33.5 (1966): 763-777.

Friedreich, N. "Zur Diagnose der Herzbeutelverwachsungen." Archiv für pathologische Anatomie und Physiologie und für klinische Medicin 29.3-4 (1864): 296-312.

Smith, S. Maynard. "Pericardial knock." British Medical Journal 1.2977 (1918): 78.

Hancock, E. W. "Subacute effusive-constrictive pericarditis." Circulation 43.2 (1971): 183-192.

Shabetai, Ralph, Noble O. Fowler, and Warren G. Guntheroth. "The hemodynamics of cardiac tamponade and constrictive pericarditis." The American journal of cardiology 26.5 (1970): 480-489.

Curtiss, Edward I., et al. "Pulsus paradoxus: definition and relation to the severity of cardiac tamponade." American heart journal 115.2 (1988): 391-398.

Swami, Ashwin, and David H. Spodick. "Pulsus paradoxus in cardiac tamponade: a pathophysiologic continuum." Clinical cardiology 26.5 (2003): 215-217.

Hamzaoui, Olfa, Xavier Monnet, and Jean-Louis Teboul. "Pulsus paradoxus." European Respiratory Journal 2013 42: 1696-1705

Ruskin, Jerome, et al. "Pressure-flow studies in man: effect of respiration on left ventricular stroke volume." Circulation 48.1 (1973): 79-85.

Wong, Frankie WH. "Pulsus paradoxus in ventilated and non-ventilated patients." Dynamics 18.3 (2007): 16-18.

Khasnis, A., and Yash Lokhandwala. "Clinical signs in medicine: pulsus paradoxus." Journal of postgraduate medicine 48.1 (2002): 46.

Möller, C. T., C. G. Schoonbee, and G. ROSENDORFF. "Haemodynamics of cardiac tamponade during various modes of ventilation." British Journal of Anaesthesia 51.5 (1979): 409-415.

Wagner, Henry R. "Paradoxical pulse: 100 years later." American Journal of Cardiology 32.1 (1973): 91-92.

Tamburro, Robert F., John C. Ring, and Kimberly Womback. "Detection of pulsus paradoxus associated with large pericardial effusions in pediatric patients by analysis of the pulse-oximetry waveform." Pediatrics 109.4 (2002): 673-677.

Friedman, Howard S., et al. "The electrocardiographic features of acute cardiac tamponade." Circulation 50.2 (1974): 260-265.

Eisenberg, Mark J., et al. "The diagnosis of pericardial effusion and cardiac tamponade by 12-lead ECG: a technology assessment." Chest 110.2 (1996): 318-324.

Badiger, Sharan, Prema T. Akkasaligar, and M. S. Biradar. "Electrocardiography–pericarditis, pericardial effusion and cardiac tamponade." International Journal of Internal Medicine1.4 (2012): 37-41.

Pérez-Casares, Alejandro, et al. "Echocardiographic evaluation of Pericardial effusion and Cardiac Tamponade." Frontiers in pediatrics 5 (2017): 79.